Abstract
The increased demand on protein folding in the endoplasmic reticulum (ER) during bacterial infection activates the unfolded protein response (UPR). OCTR-1-a G protein-coupled catecholamine receptor expressed in neurons-suppresses innate immunity by downregulating a non-canonical UPR pathway and the p38 MAPK pathway. Here, we show that OCTR-1 also regulates the canonical UPR pathway, which is controlled by XBP-1, at the organismal level. Importantly, XBP-1 is not under OCTR-1 control during development, only at the adult stage. Our results indicate that the nervous system temporally controls the UPR pathway to maintain ER homeostasis during development and immune activation.
Original language | English (US) |
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Pages (from-to) | 855-860 |
Number of pages | 6 |
Journal | EMBO Reports |
Volume | 13 |
Issue number | 9 |
DOIs | |
State | Published - Sep 2012 |
Externally published | Yes |
Keywords
- ER stress
- OCTR-1
- innate immunity
- nervous system
- unfolded protein response
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Genetics